Valve prolapse in Ischemic Mitral Regurgitation: pathogenesis, surgical timing and strategy.
Spadaccio Cristiano MD, PhD1, Antonio Nenna MD2, Al-Attar Nawwar MD,PhD1,Chello Massimo MD2, Lusini Mario MD, PhD2, Barbato Raffaele MD2,Acar Christophe MD, PhD3 and Nappi Francesco MD4.
1Department of Cardiothoracic Surgery, Golden Jubilee National Hospital, Clydebank, Glasgow, United Kingdom
2Department of Cardiovascular Surgery University Campus Bio-Medico of Rome, Italy,
3Department of Cardiovascular Surgery, Hôpital de la Salpétrière, Paris, France
4Cardiac Surgery Centre Cardiologique du Nord de Saint-Denis, Paris, France
The purpose of this study was to analyze the presence and surgical characteristics of prolapse in ischemic mitral valve regurgitation (IMR) and to elucidate its mechanisms and potential surgical strategies for its correction
Out of 226 patients undergoing surgical correction of IMR, we identified a prolapse in 75 patients (33,1% mean age 64,1 ± 11 years, 51 males 24 females). All patients had a recent or past history of coronary disease with an evidence of ischemic damage of myocardial wall or papillary muscle. Patients underwent a combined operation of mitral valve repair, using Carpentier’s techniques, and coronary revascularization, using an internal thoracic artery graft. Patients showing typical myxomatous alterations of the mitral valve or signs of rheumatic diseases were excluded. Surgical anatomy was evaluated and perioperative echocardiographic data were recorded. Patients were clinically and echocardiographically followed-up and data retrospectively reviewed.
Follow up was prolonged up to 11 years (mean 6,5 ± 2,1 years). 23 patients (30,6 %) were operated within 60 days following acute myocardial infarction. The diagnosis of prolapse had been overlooked by echography in nine cases (12%). A commissural area was involved as the site of prolapse in 45 cases (60%). The mechanism of prolapse was a papillary muscle (PM) lesion in 66 cases (88%) (Anterior PM: n=15, Posterior PM n = 50) or a chordal lesion in 9 cases (12%). PM injury included elongation (n=24), or rupture (total n=5, partial n=25, incomplete n=12). The operative technique was mitral valve repair with Carpentier’s techniques in 62 cases (92,5%) or replacement in 7 cases (9,3%). In patients operated more than 3 months after the acute ischemic event, PM elongation was the most frequent mechanism. In-hospital mortality was 10,7% (n=8). Overall survival was 71 ± 5,4% at 5 years and 42,2 ± 8,6% at 10 years, respectively. Freedom from cardiac related events was 73,4 ± 5,2% and 48 ± 9,2% at 5 and 10 years, respectively. Freedom from reoperation was 90,6 ± 3,6% and 71,6 ± 6,8% at 5 and 10 years, respectively. PM elongation correlated with increased long-term mortality (P= 0.004). Other independent predictors of mortality were a preoperative telediastolic diameter >58 mm and elevated pulmonary systolic pressures.
Mitral valve prolapse in IMR has a relatively high incidence and its pathogenic mechanism mostly relies on PM lesion or elongation. Particular care should be taken in the preoperative echocardiographic diagnosis of this condition as it might profoundly influence the surgical strategy in these patients. Carpentier techniques and interventions on the subvalvular apparatus are effective in these situations. However, timing of surgery and geometrical parameters of the left ventricle affect long-term outcomes in these patients. PM elongation and preoperative telediastolic diameters >58 mm were associated to increased mortality and were mainly detected in patients undergoing surgery late after the acute ischemic event. From our data it could be speculated that early intervention might be preferable in this population.